Profile of Central and Effector Memory T Cells in the Progression of Chronic Human Chagas Disease

Chagas disease is a parasitic infection caused by protozoan Trypanosoma cruzi that affects approximately 11 million people in Latin America. The involvement of the host's immune response on the development of severe forms of Chagas disease has not been fully elucidated. Studies on the immune re...

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Bibliographic Details
Main Authors: Fiuza, Jacqueline Araújo, Fujiwara, Ricardo Toshio, Gomes, Juliana Assis Silva, Rocha, Manoel Otávio das Costa, Chaves, Ana Thereza, de Araújo, Fernanda Fortes, Fares, Rafaelle Christine Gomes, Teixeira-Carvalho, Andrea, Martins-Filho, Olindo de Assis, Cançado, Guilherme Grossi Lopes, Correa-Oliveira, Rodrigo
Format: Online
Language:English
Published: Public Library of Science 2009
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729721/
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Summary:Chagas disease is a parasitic infection caused by protozoan Trypanosoma cruzi that affects approximately 11 million people in Latin America. The involvement of the host's immune response on the development of severe forms of Chagas disease has not been fully elucidated. Studies on the immune response against T. cruzi infection show that the immunoregulatory mechanisms are necessary to prevent the deleterious effect of excessive immune response stimulation and consequently the fatal outcome of the disease. A recall response against parasite antigens observed in in vitro peripheral blood cell culture clearly demonstrates that memory response is generated during infection. Memory T cells are heterogeneous and differ in both the ability to migrate and exert their effector function. This heterogeneity is reflected in the definition of central (TCM) and effector memory (TEM) T cells. Our results suggest that a balance between regulatory and effectors T cells may be important for the progression and development of the disease. Furthermore, the high percentage of central memory CD4+ T cells in indeterminate patients after stimulation suggests that these cells may modulate host's inflammatory response by controlling cell migration to tissues and their effector role during chronic phase of the disease.